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Ary
The Ary (Ardat Yakshi) genes are a family of divergent genes within the Asari genome in which mutations lead to a statistically significant proclivity in development of the Ardat-Yakshi Disequilibrium. Given the seriousness of Ardat-Yakshi spectrum disorders and the disfavorable societal effects produced by Ardat-Yakshi patients, the Ary family of genes have been an intensive topic of research for the Asari biological research community for millenia. Genetic basis Given that the Ardat-Yakshi Disequilibrium leads to sterility in almost all Ardat-Yakshi patients, it is believed that mutations in the Ary genes are evolutionarily strongly selected against. Nevertheless, the relatively high prevalence of Asari that fall within the Ardat-Yakshi spectrum (~1% of the total population) argues against such a hypothesis. In a landmark correspondence, Matriarch Dilinaga posited a novel hypothesis wherein she claimed that the Ardat-Yakshi series of disorders are not caused by mutations in individual Ary genes, and instead that such mutations in individual Ary genes can confer an evolutionary fitness advantage, thus allowing single Ary mutants to propagate well throughout the Asari population. However, Dilinaga proposed that crossing two Asari with individual Ary mutations led to offspring with mutations in multiple Ary genes — and that the coincidence of dysfunction within several Ary genes concomitant within a single individual led to the development of Ardat-Yakshi Disequilibrium and sterility. Thus, there would be a constant evolution of Ardat-Yakshi Disequilibrium patients from the Asari society, with no counterselective pressure against those parents that carried single Ary mutations. This has since been ratified and this "multiple hit" theory as to the genetics of the Ardat-Yakshi Disequilibrium has been widely-accepted. This has further been affirmed by statistical reports that the Ardat-Yakshi Disequilibrium is disproportionately prevalent in pureblood families — marriage of two Asari individuals would significantly increase the chances that the subsequent child would carry copies of mutant Ary genes from both parents. In mixed marriages between an Asari and a non-Asari, the child would have to spontaneously develop mutations in an Ary gene after inheriting a single Ary mutation from the Asari parent. List of genes There are approximately fifty Ary genes with significantly strong statistical associations for development of the Ardat-Yakshi Disequilibrium. Over two hundred additional genes have been listed as Ary candidates, as they have a significant but weak association with development of Ardat-Yakshi spectrum disorders. *'Ary1': The original first gene found to be associated with the development of the Ardat-Yakshi Disequilibrium. Encodes a DNA damage repair factor specifically expressed in multipotent neural stem cells and restricted neural progenitors. Molecular role remains undefined, although deficiencies in DNA repair within neural stem cells or progenitors during development have been speculated to lead to apoptosis in progeny neurons that accumulate excessive DNA damage due to insufficient genomic protection within their parental cells. *'Ary16b1': A homologue and member of a family of closely-related neural cytoskeletal proteins in the Ary16 family (including the related Ary16a and Ary16c families). Nevertheless, only Ary16b1 is specifically associated with the Ardat-Yakshi Disequilibrium. Unusually, disease-associated Ary16b1 mutations appear to be hypermorphic in nature, leading to enhanced neuronal cytoskeletal elaborations within mutant patients and development of profuse synapses with coterminous neurons. Hypomorphic Ary16b1 mutations are believed to be associated with heritable mental retardation. *'Ary28': Encodes an orphan protein homologous to epigenetic regulators of the ATP-dependent chromatin remodeller families. Despite sequence homology to ATP-dependent chromatin remodellers, the encoded protein does not exhibit significant affinity for ATP nor chromatin decompaction activity in vitro. Nevertheless, genome-wide epigenetic analyses in Ary28 mutant patients reveals marked DNA demethylation and decreased affinity of heterochromatin-associated factors to the net genome. Molecular mechanism for epigenetic dysregulation remains undetermined. Category:RelentlessRecusant